Antidepressant & Psychedelic Drug Interaction Chart

Total Page:16

File Type:pdf, Size:1020Kb

Load more

SpiritPharmacist.com 12/19 Antidepressant & Psychedelic Drug Interaction Chart This chart is not intended to be used to make medical decisions and is for informational purposes only. It was constructed using data whenever possible, although extrapolation from known information was also used to inform risk. Any decision to start, stop, or taper medication and/or use psychedelic drugs should be made in conjunction with your healthcare provider(s). It is recommended to not perform any illicit activity. Antidepressant Phenethylamines Tryptamines MAOI-containing Ketamine Ibogaine -MDMA, mescaline -Psilocybin, LSD -Ayahuasca, Syrian Rue SSRIs Taper & discontinue at least 2 Consider taper & Taper & discontinue at least 2 Has been studied and Taper & discontinue at · Paroxetine (Paxil) weeks prior (all except discontinuation at least 2 weeks weeks prior (all except found effective both with least 2 weeks prior (all · Sertraline (Zoloft) fluoxetine) or 6 weeks prior prior (all except fluoxetine) or 6 fluoxetine) or 6 weeks prior and without concurrent except fluoxetine) or 6 · Citalopram (Celexa) (fluoxetine only) due to loss of weeks prior (fluoxetine only) (fluoxetine only) due to use of antidepressants weeks prior (fluoxetine · Escitalopram (Lexapro) psychedelic effect due to potential loss of potential risk of serotonin only) due to risk of · Fluxoetine (Prozac) psychedelic effect syndrome additive QTc interval · Fluvoxamine (Luvox) MDMA is unable to cause Recommended prolongation, release of serotonin when the Chronic antidepressant use may Life threatening toxicities can to be used in conjunction arrhythmias, or SPARI serotonin reuptake pump is result in down-regulation of occur with these with oral antidepressants cardiotoxicity · Vibryyd (Vilazodone) blocked. This leads to drastically 5HT2A receptors and blunted combinations and is strictly by esketamine · Trintellix (Vortioxetine) reduced effects [1-7] psychedelic experiences [8, 9]. contraindicated [10, 11] manufacturer Some antidepressants are This does not seem to affect liver (CYP2D6) inhibitors SNRI psilocybin for some and have been shown to ·Venlafaxine (Effexor) double ibogaine blood ·Duloxetine (Cymbalta) concentrations [12] ·Desvenlafaxine (Pristiq) ·Levomilnacipran (Fetzima) DNRI Increased effects of MDMA with Loss of effect not predicted to Taper & discontinue at least 2 Taper & discontinue at · Bupropion (Wellbutrin) higher blood concentrations for occur, consider taper & weeks prior due to potential least 2 weeks prior to use. longer [13]. May increase risk of discontinuation depending on of adverse effects, however May increase risk of seizures in combination. Caution goals of psychedelic use serotonin syndrome unlikely seizures in combination. in combination. Consider taper to occur [14] & discontinuation of bupropion. CYP2D6 inhibitor with Alternatively, a 25% reduced potential to increase dose of MDMA if bupropion is ibogaine blood continued. cocnentrations · Mirtazapine (Remeron) Taper & discontinue at least 2 weeks prior due to loss of psychedelic effect Taper & discontinue at least 2 week prior due to Mirtazapine does not block the serotonin reuptake pump like SSRI, SPARI, or SNRI antidepressants. It risk of additive QTc blocks the 5HT2A receptor, thus is predicted to cause a blunting or loss of psychedelic effects. It has interval prolongation, not been associated with serotonin syndrome with MAOIs [14] arrhythmias, or cardiotoxicity SSRI = selective serotonin reuptake inhibitor SPARI = serotonin partial agonist and reuptake inhibitor SNRI = serotonin norepinephrine reuptake inhibitor DNRI = dopamine norepinephrine reuptake inhibitor MAOI = monoamine oxidase inhibitor SERT = serotonin reuptake pump 5HT2A = serotonin 2A receptor 1 SpiritPharmacist.com 12/19 Antidepressant Phenethylamines Tryptamines MAOI-containing Ketamine Ibogaine -MDMA, mescaline -Psilocybin, LSD -Ayahuasca, Syrian Rue Tricyclic Antidepressant (TCA) Taper & discontinue at Consider taper & Taper & discontinue at least 2 Has been studied Taper & discontinue at · Amitriptyline (Elavil) least 2 weeks prior due to discontinuation at least 2 weeks prior due to potential risk of and found effective least 2 weeks prior due · Nortriptyline (Pamelor) loss of psychedelic effect weeks prior due to potential serotonin syndrome. Risk is both with and to risk of additive QTc · Clomipramine (Anafranil) intensified effects highest with clomipramine, without concurrent interval prolongation, · Imipramine (Tofranil) MDMA is unable to cause imipramine, and chlorpheniramine use of arrhythmias, or · Desipramine (Norpramin) release of serotonin when Chronic TCA use was reported [14] antidepressants cardiotoxicity · Chlorpheniramine the serotonin reuptake to increase the subjective pump is blocked. This leads effects of LSD [15] Life threatening toxicities can Some antidepressants to drastically reduced occur with these combinations and Recommended are liver (CYP2D6) effects is strictly contraindicated to be used in inhibitors and have conjunction with been shown to double oral antidepressants ibogaine blood by esketamine concentrations · Trazodone (Desyrel) Taper & discontinue at least 5 days prior due to loss of psychedelic effect manufacturer Taper & discontinue at least 1 week prior due Trazodone blocks 5HT2A receptors at lower doses (25-150mg) and starts blocking the serotonin to risk of additive QTc reuptake pump (SERT) at >150mg [14]. It has an active metabolite that also blocks 5HT2A receptors interval prolongation, as well as modulating many other 5HT receptors arrhythmias, or cardiotoxicity · Buspirone (Buspar) Taper & discontinue at least 5 days prior due to loss of psychedelic effect Taper & discontinue at least 5 days prior due Buspirone is a non-psychedelic partial agonist at serotonin receptors, thus may display blunting of to potential risk of psychedelic effects due to competitive inhibition when used in combination with psychedelics [16]. toxicity It does not inhibit the reuptake of nor release neurotransmitters, thus risk of serotonin syndrome with MAOIs is low MAO-A Inhibitors* Taper & discontinue at Consider taper & Taper & discontinue at least 2 Taper & discontinue at · Phenelzine (Nardil) least 2 weeks prior due to discontinuation at least 2 weeks prior least 10 days prior due · Isocarboxazid (Parnate) potential risk of serotonin weeks prior due to potential to potential risk of · Tranylcypromine (Marplan) syndrome or hypertensive loss of psychedelic effect [15] Additive use of MAOIs may cause toxicity [20] · Moclobemide crisis [17] intensified experiences or Contraindicated with cardiovascular collapse (fainting or *chronic use tryptamine 5-MeO-DMT [18, dangerously low blood pressure) 19] MAO-B inhibitors Intensified effects, risk of Intensified effects possible, risk · Selegeline (Emsam) serotonin syndrome at of serotonin syndrome at doses ≥9mg/day doses ≥9mg/day with 5-MeO- DMT; psilocybin or LSD likely Taper & discontinue at have low risks of physical least 2 weeks prior, toxicity in combination especially if dose ≥9mg/day SSRI = selective serotonin reuptake inhibitor SPARI = serotonin partial agonist and reuptake inhibitor SNRI = serotonin norepinephrine reuptake inhibitor DNRI = dopamine norepinephrine reuptake inhibitor MAOI = monoamine oxidase inhibitor SERT = serotonin reuptake pump 5HT2A = serotonin 2A receptor 2 SpiritPharmacist.com 12/19 References: 1. Farre, M., et al., Pharmacological interaction between 3,4-methylenedioxymethamphetamine (ecstasy) and paroxetine: pharmacological effects and pharmacokinetics. J Pharmacol Exp Ther, 2007. 323(3): p. 954-62. 2. Hysek, C.M., et al., Duloxetine inhibits effects of MDMA ("ecstasy") in vitro and in humans in a randomized placebo-controlled laboratory study. PLoS One, 2012. 7(5): p. e36476. 3. Liechti, M.E. and F.X. Vollenweider, The serotonin uptake inhibitor citalopram reduces acute cardiovascular and vegetative effects of 3,4- methylenedioxymethamphetamine ('Ecstasy') in healthy volunteers. J Psychopharmacol, 2000. 14(3): p. 269-74. 4. Piper, B.J., et al., Dissociation of the neurochemical and behavioral toxicology of MDMA ('Ecstasy') by citalopram. Neuropsychopharmacology, 2008. 33(5): p. 1192-205. 5. Stein, D.J. and J. Rink, Effects of "Ecstasy" blocked by serotonin reuptake inhibitors. J Clin Psychiatry, 1999. 60(7): p. 485. 6. Tancer, M. and C.E. Johanson, The effects of fluoxetine on the subjective and physiological effects of 3,4-methylenedioxymethamphetamine (MDMA) in humans. Psychopharmacology (Berl), 2007. 189(4): p. 565-73. 7. Gudelsky, G.A. and J.F. Nash, Carrier-mediated release of serotonin by 3,4-methylenedioxymethamphetamine: implications for serotonin-dopamine interactions. J Neurochem, 1996. 66(1): p. 243-9. 8. Bonson, K.R., J.W. Buckholtz, and D.L. Murphy, Chronic administration of serotonergic antidepressants attenuates the subjective effects of LSD in humans. Neuropsychopharmacology, 1996. 14(6): p. 425-36. 9. Carhart-Harris, R.L. and D.J. Nutt, Serotonin and brain function: a tale of two receptors. Journal of Psychopharmacology (Oxford, England), 2017. 31(9): p. 1091-1120. 10. Callaway, J.C. and C.S. Grob, Ayahuasca preparations and serotonin reuptake inhibitors: a potential combination for severe adverse interactions. J Psychoactive Drugs, 1998. 30(4): p. 367-9. 11. Malcolm, B.J. and K.C. Lee, Ayahuasca: An ancient sacrament for treatment of contemporary psychiatric illness? Ment Health Clin, 2017. 7(1): p. 39-45. 12. Glue, P., et al., Influence of CYP2D6 activity on the pharmacokinetics and pharmacodynamics
Recommended publications
  • Dextromethorphan Attenuates Sensorineural Hearing Loss in an Animal Model and Population-Based Cohort Study

    Dextromethorphan Attenuates Sensorineural Hearing Loss in an Animal Model and Population-Based Cohort Study

    International Journal of Environmental Research and Public Health Article Dextromethorphan Attenuates Sensorineural Hearing Loss in an Animal Model and Population-Based Cohort Study Hsin-Chien Chen 1,* , Chih-Hung Wang 1,2 , Wu-Chien Chien 3,4 , Chi-Hsiang Chung 3,4, Cheng-Ping Shih 1, Yi-Chun Lin 1,2, I-Hsun Li 5,6, Yuan-Yung Lin 1,2 and Chao-Yin Kuo 1 1 Department of Otolaryngology-Head and Neck Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan; [email protected] (C.-H.W.); [email protected] (C.-P.S.); [email protected] (Y.-C.L.); [email protected] (Y.-Y.L.); [email protected] (C.-Y.K.) 2 Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan 3 School of Public Health, National Defense Medical Center, Taipei 114, Taiwan; [email protected] (W.-C.C.); [email protected] (C.-H.C.) 4 Department of Medical Research, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan 5 Department of Pharmacy Practice, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan; [email protected] 6 School of Pharmacy, National Defense Medical Center, Taipei 114, Taiwan * Correspondence: [email protected]; Tel.: +886-2-8792-7192; Fax: +886-2-8792-7193 Received: 31 July 2020; Accepted: 28 August 2020; Published: 31 August 2020 Abstract: The effect of dextromethorphan (DXM) use in sensorineural hearing loss (SNHL) has not been fully examined. We conducted an animal model and nationwide retrospective matched-cohort study to explore the association between DXM use and SNHL.
  • WELLBUTRIN SR Safely and Effectively

    WELLBUTRIN SR Safely and Effectively

    HIGHLIGHTS OF PRESCRIBING INFORMATION psychosis, hallucinations, paranoia, delusions, homicidal ideation, These highlights do not include all the information needed to use aggression, hostility, agitation, anxiety, and panic, as well as suicidal WELLBUTRIN SR safely and effectively. See full prescribing ideation, suicide attempt, and completed suicide. Observe patients information for WELLBUTRIN SR. attempting to quit smoking with bupropion for the occurrence of such symptoms and instruct them to discontinue bupropion and contact a WELLBUTRIN SR (bupropion hydrochloride) sustained-release tablets, healthcare provider if they experience such adverse events. (5.2) for oral use • Initial U.S. Approval: 1985 Seizure risk: The risk is dose-related. Can minimize risk by gradually increasing the dose and limiting daily dose to 400 mg. Discontinue if WARNING: SUICIDAL THOUGHTS AND BEHAVIORS seizure occurs. (4, 5.3, 7.3) See full prescribing information for complete boxed warning. • Hypertension: WELLBUTRIN SR can increase blood pressure. Monitor blood pressure before initiating treatment and periodically during • Increased risk of suicidal thinking and behavior in children, treatment. (5.4) adolescents and young adults taking antidepressants. (5.1) • Activation of mania/hypomania: Screen patients for bipolar disorder and • Monitor for worsening and emergence of suicidal thoughts and monitor for these symptoms. (5.5) behaviors. (5.1) • Psychosis and other neuropsychiatric reactions: Instruct patients to contact a healthcare professional if such reactions occur. (5.6) --------------------------- INDICATIONS AND USAGE ---------------------------- • Angle-closure glaucoma: Angle-closure glaucoma has occurred in WELLBUTRIN SR is an aminoketone antidepressant, indicated for the patients with untreated anatomically narrow angles treated with treatment of major depressive disorder (MDD). (1) antidepressants.
  • Concomitant Drugs Associated with Increased Mortality for MDMA Users Reported in a Drug Safety Surveillance Database Isaac V

    Concomitant Drugs Associated with Increased Mortality for MDMA Users Reported in a Drug Safety Surveillance Database Isaac V

    www.nature.com/scientificreports OPEN Concomitant drugs associated with increased mortality for MDMA users reported in a drug safety surveillance database Isaac V. Cohen1, Tigran Makunts2,3, Ruben Abagyan2* & Kelan Thomas4 3,4-Methylenedioxymethamphetamine (MDMA) is currently being evaluated by the Food and Drug Administration (FDA) for the treatment of post-traumatic stress disorder (PTSD). If MDMA is FDA-approved it will be important to understand what medications may pose a risk of drug– drug interactions. The goal of this study was to evaluate the risks due to MDMA ingestion alone or in combination with other common medications and drugs of abuse using the FDA drug safety surveillance data. To date, nearly one thousand reports of MDMA use have been reported to the FDA. The majority of these reports include covariates such as co-ingested substances and demographic parameters. Univariate and multivariate logistic regression was employed to uncover the contributing factors to the reported risk of death among MDMA users. Several drug classes (MDMA metabolites or analogs, anesthetics, muscle relaxants, amphetamines and stimulants, benzodiazepines, ethanol, opioids), four antidepressants (bupropion, sertraline, venlafaxine and citalopram) and olanzapine demonstrated increased odds ratios for the reported risk of death. Future drug–drug interaction clinical trials should evaluate if any of the other drug–drug interactions described in our results actually pose a risk of morbidity or mortality in controlled medical settings. 3,4-Methylenedioxymethamphetamine (MDMA) is currently being evaluated by the Food and Drug Adminis- tration (FDA) for the treatment of posttraumatic stress disorder (PTSD). During the past two decades, “ecstasy” was illegally distributed and is purported to contain MDMA, but because the market is unregulated this “ecstasy” may actually contain adulterants or no MDMA at all1.
  • Canadian Stroke Best Practice Recommendations

    Canadian Stroke Best Practice Recommendations

    CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MOOD, COGNITION AND FATIGUE FOLLOWING STROKE Table 1C: Summary Table for Selected Pharmacotherapy for Post-Stroke Depression Update 2019 Lanctôt KL, Swartz RH (Writing Group Chairs) on Behalf of the Canadian Stroke Best Practice Recommendations Mood, Cognition and Fatigue following Stroke Writing Group and the Canadian Stroke Best Practice and Quality Advisory Committee, in collaboration with the Canadian Stroke Consortium © 2019 Heart & Stroke Heart and Stroke Foundation Mood, Cognition and Fatigue following Stroke Canadian Stroke Best Practice Recommendations Table 1C Table 1C: Summary Table for Selected Pharmacotherapy for Post-Stroke Depression This table provides a summary of the pharmacotherapeutic properties, side effects, drug interactions and other important information on selected classes of medications available for use in Canada and more commonly recommended for post-stroke depression. This table should be used as a reference guide by health care professionals when selecting an appropriate agent for individual patients. Patient compliance, patient preference and/or past experience, side effects, and drug interactions should all be taken into consideration during decision-making, in addition to other information provided in this table and available elsewhere regarding these medications. Selective Serotonin Reuptake Inhibitors (SSRI) Serotonin–norepinephrine reuptake Other inhibitors (SNRI) Medication *citalopram – Celexa *duloxetine – Cymbalta methylphenidate – Ritalin (amphetamine)
  • Review Paper Monoamine Oxidase Inhibitors: a Review Concerning Dietary Tyramine and Drug Interactions

    Review Paper Monoamine Oxidase Inhibitors: a Review Concerning Dietary Tyramine and Drug Interactions

    PsychoTropical Commentaries (2016) 1:1 – 90 © Fernwell Publications Review Paper Monoamine Oxidase Inhibitors: a Review Concerning Dietary Tyramine and Drug Interactions PK Gillman PsychoTropical Research, Bucasia, Queensland, Australia Abstract This comprehensive monograph surveys original data on the subject of both dietary tyramine and drug interactions relevant to Monoamine Oxidase Inhibitors (MAOIs), about which there is much outdated, incorrect and incomplete information in the medical literature and elsewhere. Fewer foods than previously supposed have problematically high tyramine levels because international food hygiene regulations have improved both production and handling. Cheese is the only food that has, in the past, been associated with documented fatalities from hypertension, and now almost all ‘supermarket’ cheeses are perfectly safe in healthy-sized portions. The variability of sensitivity to tyramine between individuals, and the sometimes unpredictable amount of tyramine content in foods, means a little knowledge and care are still advised. The interactions between MAOIs and other drugs are now well understood, are quite straightforward, and are briefly summarized here (by a recognised expert). MAOIs have no apparently clinically relevant pharmaco-kinetic interactions, and the only significant pharmaco-dynamic interaction, other than the ‘cheese reaction’ (caused by indirect sympatho-mimetic activity [ISA], is serotonin toxicity ST (aka serotonin syndrome) which is now well defined and straightforward to avoid by not co-administering any drug with serotonin re-uptake inhibitor (SRI) potency. There are no therapeutically used drugs, other than SRIs, that are capable of inducing serious ST with MAOIs. Anaesthesia is not contra- indicated if a patient is taking MAOIs. Most of the previously held concerns about MAOIs turn out to be mythical: they are either incorrect, or over-rated in importance, or stem from apprehensions born out of insufficient knowledge.
  • Download Product Insert (PDF)

    Download Product Insert (PDF)

    PRODUCT INFORMATION Tyramine Item No. 18601 CAS Registry No.: 51-67-2 Formal Name: 4-(2-aminoethyl)-phenol Synonyms: 2-(4-Hydroxyphenyl)ethylamine, NSC 249188, p-Tyramine, NH2 Uteramine MF: C8H11NO FW: 137.2 HO Purity: ≥98% UV/Vis.: λmax: 224, 278 nm Supplied as: A crystalline solid Storage: -20°C Stability: ≥2 years Information represents the product specifications. Batch specific analytical results are provided on each certificate of analysis. Laboratory Procedures Tyramine is supplied as a crystalline solid. A stock solution may be made by dissolving the tyramine in the solvent of choice. Tyramine is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of tyramine in these solvents is approximately 5, 20, and 25 mg/ml, respectively. Tyramine is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, tyramine should first be dissolved in DMF and then diluted with the aqueous buffer of choice. Tyramine has a solubility of approximately 0.5 mg/ml in a 1:1 solution of DMF:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day. Description Tyramine is a tyrosine-derived endogenous and dietary monoamine and trace amine-associated receptor 1-3 1 (TAAR1) agonist. It activates TAAR1 (EC50s = 0.08, 0.69, and 2.26 µM for rat, mouse, and human-rat chimera receptors, respectively).1 Tyramine also inhibits the release of norepinephrine and dopamine in 4 isolated rat caudate nucleus (IC50s = 40.6 and 119 nM, respectively).
  • A Quick Guide to Drugs and Alcohol

    A Quick Guide to Drugs and Alcohol

    A QUICK GUIDE TO Drugs & Alcohol THIRD EDITION by the National Drug and Alcohol Research Centre (NDARC) Drug Info is a partnership between the State Library of New South Wales and NSW Health. www.druginfo.sl.nsw.gov.au Disclaimer The contents of this book are intended for information purposes only. Every efort has been made to ensure that the information is correct at the time of publication. Drug Info does not ofer any information in this book as a tool for treatment, counselling or legal advice. Drug Info recommends that prior to making any decision based on any information in this book, you should obtain independent professional legal or medical advice. Websites and information about service providers referred to in the publication have been selected to provide relevant and up-to-date information as at the date of publication. Drug Info accepts no responsibility for the content of websites and does not endorse any specifc services ofered by providers. A Quick Guide to Drugs & Alcohol, third edition, September 2017 Published by Drug Info, State Library of NSW © Copyright Library Council of NSW and NSW Ministry of Health, 2017 ISBN 0 7313 7239 5 (print) ISBN 0 7313 7240 9 (online) Printed in Australia by SEED Print, using Spicers Paper Monza Recycled Satin 350 gsm and Impress Matt 115 gsm. Monza Recycled contains 99% recycled fbre and is FSC® Mix Certifed, Impress Matt is FSC® Mix Certifed. P&D-4660-9/2017 ECSTASY E, pills, eccy, XTC, MDMA, pingas, Adam, X 7 Ecstasy is a derivative of methamphetamine (the active ingredient is 3, 4-methylenedioxymethamphetamine, abbreviated to MDMA).
  • Pharmacokinetic Interactions of Drugs with St John's Wort

    Pharmacokinetic Interactions of Drugs with St John's Wort

    http://www.paper.edu.cn Pharmacokinetic interactions of Journal of Psychopharmacology 18(2) (2004) 262–276 © 2004 British Association drugs with St John’s wort for Psychopharmacology ISSN 0269-8811 SAGE Publications Ltd, London, Thousand Oaks, CA and New Delhi 10.1177/0269881104042632 Shufeng Zhou Department of Pharmacy, Faculty of Science, National University of Singapore, Singapore. Eli Chan Department of Pharmacy, Faculty of Science, National University of Singapore, Singapore. Shen-Quan Pan Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore. Min Huang Institute of Clinical Pharmacology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510089, PR China. Edmund Jon Deoon Lee Department of Pharmacology, Faculty of Medicine, National University of Singapore, Singapore. Abstract There is a worldwide increasing use of herbs which are often cancer patients receiving irinotecan treatment. St John’s wort did not administered in combination with therapeutic drugs, raising the alter the pharmacokinetics of tolbutamide, but increased the incidence potential for herb–drug interactions. St John’s wort (Hypericum of hypoglycaemia. Several cases have been reported that St John’s wort perforatum) is one of the most commonly used herbal antidepressants. A decreased cyclosporine blood concentration leading to organ rejection. literature search was performed using Medline (via Pubmed), Biological St John’s wort caused breakthrough bleeding and unplanned pregnancies Abstracts, Cochrane Library, AMED, PsycINFO and Embase (all from their when used concomitantly with oral contraceptives. It also caused inception to September 2003) to identify known drug interaction with serotonin syndrome when coadministered with selective serotonin- St John’s wort. The available data indicate that St John’s wort is a reuptake inhibitors (e.g.
  • CYP3A4 Mediated Pharmacokinetics Drug Interaction Potential of Maha

    CYP3A4 Mediated Pharmacokinetics Drug Interaction Potential of Maha

    www.nature.com/scientificreports OPEN CYP3A4 mediated pharmacokinetics drug interaction potential of Maha‑Yogaraj Gugglu and E, Z guggulsterone Sarvesh Sabarathinam1, Satish Kumar Rajappan Chandra2 & Vijayakumar Thangavel Mahalingam1* Maha yogaraja guggulu (MYG) is a classical herbomineral polyherbal formulation being widely used since centuries. The aim of this study was to investigate the efect of MYG formulation and its major constituents E & Z guggulsterone on CYP3A4 mediated metabolism. In vitro inhibition of MYG and Guggulsterone isomers on CYP3A4 was evaluated by high throughput fuorometric assay. Eighteen Adult male Sprague–Dawley rats (200 ± 25 g body weight) were randomly divided into three groups. Group A, Group B and Group C were treated with placebo, MYG and Standard E & Z guggulsterone for 14 days respectively by oral route. On 15th day, midazolam (5 mg/kg) was administered orally to all rats in each group. Blood samples (0.3 mL) were collected from the retro orbital vein at 0.25, 0.5, 0.75, 1, 2, 4, 6, 12 and 24 h of each rat were collected. The fndings from the in vitro & in vivo study proposed that the MYG tablets and its guggulsterone isomers have drug interaction potential when consumed along with conventional drugs which are CYP3A4 substrates. In vivo pharmacokinetic drug interaction study of midazolam pointed out that the MYG tablets and guggulsterone isomers showed an inhibitory activity towards CYP3A4 which may have leads to clinically signifcant interactions. Te use of alternative medicine such as herbal medicines, phytonutrients, ayurvedic products and nutraceuticals used widely by the majority of the patients for their primary healthcare needs.
  • Pharmacology and Toxicology of Amphetamine and Related Designer Drugs

    Pharmacology and Toxicology of Amphetamine and Related Designer Drugs

    Pharmacology and Toxicology of Amphetamine and Related Designer Drugs U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service • Alcohol Drug Abuse and Mental Health Administration Pharmacology and Toxicology of Amphetamine and Related Designer Drugs Editors: Khursheed Asghar, Ph.D. Division of Preclinical Research National Institute on Drug Abuse Errol De Souza, Ph.D. Addiction Research Center National Institute on Drug Abuse NIDA Research Monograph 94 1989 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol, Drug Abuse, and Mental Health Administration National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 For sale by the Superintendent of Documents, U.S. Government Printing Office Washington, DC 20402 Pharmacology and Toxicology of Amphetamine and Related Designer Drugs ACKNOWLEDGMENT This monograph is based upon papers and discussion from a technical review on pharmacology and toxicology of amphetamine and related designer drugs that took place on August 2 through 4, 1988, in Bethesda, MD. The review meeting was sponsored by the Biomedical Branch, Division of Preclinical Research, and the Addiction Research Center, National Institute on Drug Abuse. COPYRIGHT STATUS The National Institute on Drug Abuse has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other matieral in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors.
  • From Sacred Plants to Psychotherapy

    From Sacred Plants to Psychotherapy

    From Sacred Plants to Psychotherapy: The History and Re-Emergence of Psychedelics in Medicine By Dr. Ben Sessa ‘The rejection of any source of evidence is always treason to that ultimate rationalism which urges forward science and philosophy alike’ - Alfred North Whitehead Introduction: What exactly is it that fascinates people about the psychedelic drugs? And how can we best define them? 1. Most psychiatrists will define psychedelics as those drugs that cause an acute confusional state. They bring about profound alterations in consciousness and may induce perceptual distortions as part of an organic psychosis. 2. Another definition for these substances may come from the cross-cultural dimension. In this context psychedelic drugs may be recognised as ceremonial religious tools, used by some non-Western cultures in order to communicate with the spiritual world. 3. For many lay people the psychedelic drugs are little more than illegal and dangerous drugs of abuse – addictive compounds, not to be distinguished from cocaine and heroin, which are only understood to be destructive - the cause of an individual, if not society’s, destruction. 4. But two final definitions for psychedelic drugs – and those that I would like the reader to have considered by the end of this article – is that the class of drugs defined as psychedelic, can be: a) Useful and safe medical treatments. Tools that as adjuncts to psychotherapy can be used to alleviate the symptoms and course of many mental illnesses, and 1 b) Vital research tools with which to better our understanding of the brain and the nature of consciousness. Classifying psychedelic drugs: 1,2 The drugs that are often described as the ‘classical’ psychedelics include LSD-25 (Lysergic Diethylamide), Mescaline (3,4,5- trimethoxyphenylathylamine), Psilocybin (4-hydroxy-N,N-dimethyltryptamine) and DMT (dimethyltryptamine).
  • Grapefruit Juice and Psychotropics: How to Avoid Potential Interactions

    Grapefruit Juice and Psychotropics: How to Avoid Potential Interactions

    Savvy Psychopharmacology Grapefruit juice and psychotropics: How to avoid potential interactions Danielle L. Bishop, PharmD, BCPP s. H, age 42, was given a diagnosis she reports feeling much better during a fol- of bipolar disorder 10 years ago and low-up call and she makes an appointment Mhas been taking carbamazepine, to have her carbamazepine level rechecked 1,200 mg/d, and olanzapine, 10 mg/d, for the in a week. past 2 years. She has not experienced a mood episode while on this regimen, and her car- Although grapefruit products are high in bamazepine level was 9.2 μg/mL 6 months vitamins and low in calories, they can be Vicki L. Ellingrod, ago. The only adverse effect she experienced associated with potentially serious drug PharmD, FCCP was weight gain of approximately 10 lb. interactions. The interaction between Department Editor Ms. H takes a calcium supplement, but no grapefruit juice and the calcium channel other medications. blocker felodipine was discovered inad- Ms. H reports to her psychiatrist that, for vertently >20 years ago; since that time, the past few days, she has been feeling nau- possible interactions with >85 medica- seated, fatigued, and dizzy, but has contin- tions have been identified.1 Interactions ued taking her medications as prescribed. with grapefruit products are complicated Her carbamazepine level is found to be 13.1 μg/mL. Ms. H states she has not started Practice Points any new medications or supplements; her • In general, an entire grapefruit or 8 oz serum creatinine and liver function test of juice is enough to alter a susceptible results are within normal limits.